What question did this study set out to answer?

Evaluate how indoor PM2.5 exposure affects lung inflammation, and how airway-to-lung ratios modify these effects.

May 20, 2026

D30-03 Small Airway-to-Lung Size Ratio Exacerbates Indoor PM2.5 Associated Decline in CT Metrics Associated With Lung Inflammation: A SPIROMICS Air Analysis

Key Points

Evaluate how indoor PM2.5 exposure affects lung inflammation, and how airway-to-lung ratios modify these effects.
Estimated indoor PM2.5 levels and calculated airway-to-lung ratios (ALR) using CT scans.
Analyzed parenchymal texture distributions using the 3D-AMFM method across different ALR quartiles.
Conducted longitudinal analyses for qCT metrics in relation to PM2.5 exposure over one year.
Significant increase in %GGO associated with indoor PM2.5 (β=0.04, p=0.024).
Participants in the lowest ALR quartile showed greater changes in %BV due to PM2.5 (β=0.024, p=0.001).
No significant associations found for %GGO (p=0.056) or %GGR (p=0.83) in lower ALR quartile.

Abstract

Abstract Rationale Lower airway-to-lung ratios (ALR) derived from quantitative CT (qCT) have been linked to increased risk of COPD and accelerated FEV1 decline, particularly in response to indoor fine particulate matter (PM2.5). We hypothesize that indoor PM2.5 exacerbates lung inflammation, and qCT metrics of parenchymal texture, using the 3-dimensional Adaptive Multiple Feature Method (3D-AMFM), will provide greater sensitivity to evaluate these changes. We investigated the relationship between parenchymal texture distributions and indoor PM2.5 exposures in participants enrolled in SPIROMICS Air. We further evaluated the impact of ALR in modifying the associations between PM2.5 and change in parenchymal patterns over one year. Methods Indoor PM2.5 was estimated in the SPIROMICS Air study. ALR was determined by measuring the geometric mean of airway lumen diameters at 19 standard anatomic locations divided by the cube-root of total lung volume segmented from the baseline inspiratory CT scans. The 3D-AMFM approach used a Bayesian classifier to estimate the percent lung distribution across seven patterns: normal, emphysema-like, broncho-vascular bundles (BV), ground glass opacities (GGO), reticular (GGR), honey combing (HC), and consolidated. For longitudinal analyses, we stratified participants by ALR and evaluated the difference in slope of the associations (change in qCT metrics vs. indoor PM2.5), between the lowest and highest quartile, adjusting for age, sex, BMI, smoking status, pack-years, and GOLD stage. Results Data from 1054 participants were included. Indoor PM2.5 ranged from 0.04-61.61 μg/m3, following a log-normal distribution (7.68±2.46 μg/m3), and was associated with a significant increase(α = 0.05) in %GGO (β = 0.04, p = 0.024), %GGR showed similar associations with lower effect size but did not reach statistical significance (β = 0.004, p = 0.066). In the longitudinal analysis, participants in the lowest ALR quartile (≤ 0.0379) demonstrated greater associations with PM2.5 than those in the highest quartile (0.0545) for changes in: %BV (β = 0.024, p = 0.001), but not with %GGO (p = 0.056) or %GGR (p = 0.83); where β is the difference in slope between groups with PM2.5, showing that participants with the lowest ALR (i.e. greatest ALR) had significantly greater bronchovascular bundle thickening in response to indoor PM2.5. Conclusion These results support the hypothesis that indoor air pollution promotes inflammatory response in the parenchyma, and that ALR modifies participant response. Ongoing analyses using vascular and airway-specific qCT metrics aim to further characterize these responses and will provide additional insights on the nature of the changes in the bronchovascular bundle metrics. This abstract is funded by: SPIROMICS was supported by contracts from the NIH/NHLBI (HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C, 75N92024D00012), grants from the NIH/NHLBI (U01HL137880, U24HL141762, R01HL182622, R01HL144718, and R01HL093081), and supplemented by contributions made through the Foundation for the NIH and the COPD Foundation from Amgen; AstraZeneca/MedImmune; Bayer; Bellerophon Therapeutics; Boehringer-Ingelheim Pharmaceuticals, Inc.; Bristol Myers Squibb; Chiesi Farmaceutici S.p.A.; Forest Research Institute, Inc.; Genentech; GlaxoSmithKline; Grifols Therapeutics, Inc.; Ikaria, Inc.; MGC Diagnostics; Novartis Pharmaceuticals Corporation; Nycomed GmbH; Polarean; ProterixBio; Regeneron Pharmaceuticals, Inc.; Sanofi; Sunovion; Takeda Pharmaceutical Company; Theravance Biopharma; Verona; and Mylan/Viatris.

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